Two Isoforms of Yersinia pestis Plasminogen Activator Pla: Intraspecies Distribution, Intrinsic Disorder Propensity, and Contribution to Virulence

Plague is a re-emerging zoonotic disease caused by the bacterium Yersinia pestis. The disease has caused periodic global devastation since the first outbreak in the 6th century. Two months after a suspected plague outbreak in Nyimba district, samples were collected from 94 livestock (goats and pigs), 25 rodents, 6 shrews and 33 fleas. Enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR) techniques were used to investigate the presence of Y. pestis, which showed that 16.0% (4/25) of rodents, 16.7% (1/6) of shrews ( Crocidura spp) and 6.0% (5/83) of goats were positive for IgG antibodies against Fraction 1 antigen of Y. pestis. Plasminogen activator (Pla) gene (DNA) of Y. pestis was detected in five pools containing 36.4% (12/33) fleas collected from pigs (n = 4), goats (n = 5) and rodents (n = 3). The detection of Pla gene in fleas and IgG antibodies against Fraction1 antigen in rodents, shrews and goats suggest that Y. pestis had been present in the study area in the recent past.

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Further characterization of a highly attenuated Yersinia pestis CO92 mutant deleted for the genes encoding Braun lipoprotein and plasminogen activator protease in murine alveolar and primary human macrophages

Microbial Pathogenesis ◽

10.1016/j.micpath.2015.02.005 ◽

2015 ◽

Vol 80 ◽

pp. 27-38 ◽

Cited By ~ 7

Author(s):

Christina J. van Lier ◽

Bethany L. Tiner ◽

Sadhana Chauhan ◽

Vladimir L. Motin ◽

Eric C. Fitts ◽

...

Keyword(s):

Yersinia Pestis ◽

Plasminogen Activator ◽

Human Macrophages ◽

Genes Encoding

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Yersinia pestis Caf1 Protein: Effect of Sequence Polymorphism on Intrinsic Disorder Propensity, Serological Cross-Reactivity and Cross-Protectivity of Isoforms

PLoS ONE ◽

10.1371/journal.pone.0162308 ◽

2016 ◽

Vol 11 (9) ◽

pp. e0162308 ◽

Cited By ~ 2

Author(s):

Pavel Kh. Kopylov ◽

Mikhail E. Platonov ◽

Vitaly G. Ablamunits ◽

Tat’yana I. Kombarova ◽

Sergey A. Ivanov ◽

...

Keyword(s):

Yersinia Pestis ◽

Intrinsic Disorder ◽

Cross Reactivity ◽

Sequence Polymorphism

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Nucleotide sequence of the plasminogen activator gene of Yersinia pestis: relationship to ompT of Escherichia coli and gene E of Salmonella typhimurium.

Infection and Immunity ◽

10.1128/iai.57.5.1517-1523.1989 ◽

1989 ◽

Vol 57 (5) ◽

pp. 1517-1523 ◽

Cited By ~ 87

Author(s):

O A Sodeinde ◽

J D Goguen

Keyword(s):

Escherichia Coli ◽

Nucleotide Sequence ◽

Salmonella Typhimurium ◽

Yersinia Pestis ◽

Plasminogen Activator

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Direct Transcriptional Control of the Plasminogen Activator Gene of Yersinia pestis by the Cyclic AMP Receptor Protein

Journal of Bacteriology ◽

10.1128/jb.00972-07 ◽

2007 ◽

Vol 189 (24) ◽

pp. 8890-8900 ◽

Cited By ~ 33

Author(s):

Tae-Jong Kim ◽

Sadhana Chauhan ◽

Vladimir L. Motin ◽

Ee-Been Goh ◽

Michele M. Igo ◽

...

Keyword(s):

Cyclic Amp ◽

Binding Site ◽

Yersinia Pestis ◽

Plasminogen Activator ◽

Gene Networks ◽

Physiological Role ◽

Regulatory Control ◽

Global Network ◽

Receptor Protein ◽

Gene Drive

ABSTRACT Horizontal gene transfer events followed by proper regulatory integration of a gene drive rapid evolution of bacterial pathogens. A key event in the evolution of the highly virulent plague bacterium Yersinia pestis was the acquisition of plasmid pPCP1, which carries the plasminogen activator gene, pla. This promoted the bubonic form of the disease by increasing bacterial dissemination from flea bite sites and incidentally enhanced replication in respiratory airways during pneumonic infection. We determined that expression of pla is controlled by the global regulator cyclic AMP (cAMP) receptor protein (Crp). This transcription factor is well conserved among distantly related bacteria, where it acts as a soluble receptor for the ubiquitous signaling molecule cAMP and controls a global network of metabolic and stress-protective genes. Crp has a similar physiological role in Y. pestis since loss of its function resulted in an inability to metabolize a variety of nonglucose substrates. Activation of pla expression requires a transcription activation element of the pla promoter that serves as a Crp binding site. Crp interaction with this site was demonstrated to occur only in the presence of cAMP. Alteration of the Crp binding site nucleotide sequence prevented in vitro formation of Crp-DNA complexes and inhibited in vivo expression of pla. The placement of pla under direct regulatory control of Crp highlights how highly adapted pathogens integrate laterally acquired genes to coordinate virulence factor expression with global gene networks to maintain homeostasis through the infectious life cycle.

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